Fig. 8: Pharmacological inhibition or genetic silencing of AKT1 or RhoA alleviates MAFLD development in vivo. | Nature Communications

Fig. 8: Pharmacological inhibition or genetic silencing of AKT1 or RhoA alleviates MAFLD development in vivo.

From: Deficiency of gluconeogenic enzyme PCK1 promotes metabolic-associated fatty liver disease through PI3K/AKT/PDGF axis activation in male mice

Fig. 8

L-KO mice were fed the HFCD-HF/G for 24 weeks, and therapeutic treatments were initiated at different times. a Schematic diagram of in vivo pharmacological inhibition (b–d) and pSECC lentivirus-mediated silencing (e–g) of AKT1 or RhoA. b, c Liver weight (b), and serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), TNF-α, and IL-6 (c) (DMSO, n = 6; MK2206, n = 6; Rhosin, n = 5). d Paraffin-embedded liver sections were stained with hematoxylin and eosin, Sirius Red, or immunostained for F4/80, COL3A1, and α-SMA. Frozen sections were stained with Oil Red O. Scale bars: 50 µm. e Quantification of body weight and liver weight in pSECC-sgAkt1 and pSECC-sgRhoA L-KO mice (n = 6). f Plasma levels of total triglycerides (TG), total cholesterol (TC), and free fatty acids (FFA) (n = 6). g NAFLD activity scores of liver sections (n = 6). h Model depicting the critical role of PCK1 in controlling MAFLD progression. n was the number of biologically independent mice. Data are expressed as the mean ± SEM; n.s., not significant. p values obtained via one-way ANOVA with Tukey’s post hoc test. Source data are provided as a Source Data file.

Back to article page